Stroke (excluding haemorrhagic stroke) Flashcards
Stroke:
- Definition
- Causes
- Risk factors
- Presentation (general)
- Presentation (haemorrhagic)
- Presentation (anterior)
- Presentation (posterior)
- Investigations
DEFINITION:
- Ischaemia/infarction of the brain secondary to a disrupted blood supply (ischaemic stroke)
- Intracranial haemorrhage, with bleeding in or around the brain (haemorrhagic stroke)
CAUSES:
- Thromboembolism
- Atherosclerosis
- Shock
- Vasculitis
RISK FACTORS:
- Previous stroke or TIA
- Atrial fibrillation
- Carotid artery stenosis
- Hypertension
- Diabetes
- Raised cholesterol
- Family history
- Smoking
- Obesity
- Vasculitis
- Thrombophilia
- COCP
PRESENTATION (GENERAL):
- Sudden onset
- Focal symptoms
- Asymmetrical symptoms
- Typically negative symptoms
- Limb weakness
- Speech slurring
- Facial drooping/weakness
- Syncope
- Ataxia and vertigo (if posterior circulation infarct)
- FACT: patients will often remember they’re having a stroke!! (ie: no memory impairment)
O/E:
(UMN unilateral signs)
- Facial weakness (forehead sparring)
- Loss of power
- Hyporeflexia acutely, hyper-reflexia eventually
- Hypotonia acutely, hyper-tonia eventually
- Flaccidity acutely, rigidity and spasticity eventually
- Visual field defects (eg: homonymous hemianopia)
- Sensory loss
HAEMORRHAGIC STROKE:
- Headache
- Altered mental status
- Nausea & Vomiting
- Hypertension
- Seizures
- Focal neurological deficits (depending on location of bleed)
ANTERIOR ISCHAEMIC STROKE (TACS, PACS, LACS):
- Unilateral weakness AND/OR sensory deficit of the face, arm and leg
- Homonymous hemianopia
- Higher cerebral dysfunction (dysphasia, visuospatial disorder, neglect, agnosia)
POSTERIOR ISCHAEMIC STROKE:
- Cranial nerve palsy AND a contralateral motor/sensory deficit
- Bilateral motor/sensory deficit
- Conjugate eye movement disorder (inability to move both eyes together in a single horizontal or vertical direction, such as horizontal gaze palsy)
- Cerebellar dysfunction (e.g. vertigo and dizziness, nystagmus, ataxia, dysarthria, dysphagia)
- Isolated homonymous hemianopia (presents as visual field defects and “vision loss”)
INVESTIGATIONS:
a) Bedside
- ECG may reveal AF as cause of stroke
- BM to exclude hypoglycaemia as stroke mimic
b) Bloods
- FBC to look for infection and delirium as stroke mimic
- U&Es to look for electrolyte disturbances as this can mimic stroke; also to look for renal impairment, as this will affect drug dosing
- LFTs to check for abnormal liver function, as this can affect clotting
- Coagulation to check for bleeding risk
- HbA1c to diagnose diabetes as risk factor
- Lipid profile to diagnose hyperlipidaemia as risk factor
c) Imaging
- CT head urgently to diagnose stroke and the subtype of stroke; if ischaemic CT reveals “effacement”, loss of grey/white matter distinction and increased density of relevant blood vessel; if haemorrhagic CT reveals increased attenuation
- MRI head for better anatomical detail
- CT angiography to pinpoint the vessel involved
- CXR if aspiration pneumonia suspected
Stroke:
- Acute management of haemorrhagic stroke
- Acute management of ischaemic stroke
- Contraindications to thrombolysis
- Criteria for mechanical thrombectomy
- Complications
MANAGEMENT:
- ABCDE approach
- Urgent non-contrast CT head
a) Haemorrhagic stroke
- Stop/reverse anticoagulants (eg: Andexanet for Apixaban/Rivaroxaban; vitamin K for Warfarin)
- BP lowering with IV Labetalol 10mg, then consider GTN infusions; aim for BP < 140 mmHg systolic if < 6 hours of onset; or < 180 mmHg systolic if > 6 hours of onset
- Often no need for surgery if small bleed
- Consider decompressive hemicraniectomy (DHC) and suboccipital craniotomy if applicable
- DHC often for younger patients < 60 years old with malignant oedema; referral to neurosurgery should be done within 24 hours and the procedure completed within 48 hours of symptom onset
b) Ischaemic stroke
- Thrombolysis with synthetic tPA (eg: Alteplase is a clot-buster) if clinical presentation < 4.5 hours; then initiate aspirin 300mg OD for 14 days
- Mechanical thrombectomy mainly for large vessel occlusion (MCA mainly, can also be ICA or BA) only if presentation < 6 hours
- If thrombolysis and thrombectomy both contraindicated, continue on aspirin 300mg for 14 days, then convert to clopidogrel 75mg lifelong thereafter
CONTRAINDICATIONS TO THROMBOLYSIS:
- Intracranial bleeding (therefore CT head to exclude)
- Anticoagulant medication (eg: dabigatran, rivaroxaban, apixaban, edoxaban, LMWH etc)
- Bleeding or clotting disorders (INR >1.7 or APTT > 40)
- Stroke within the last 14 days
- Serious head injury within last 14 days
- Intracranial neoplasm, malignancy or aneurysm
- Thrombocytopenia (platelets < 50x10^9)
CRITERIA FOR MECHANICAL THROMBECTOMY:
- Terminal ICA occlusion
- MCA occlusion (M1 or proximal M2)
- Basilar artery occlusion
- Presentation < 6 hours from onset
- No significant early ischaemic changes on imaging
- NIHSS score of 6 or more
COMPLICATIONS FOLLOWING STROKE:
- Mortality and morbidity
- Recurrent stroke due to unaddressed risk factors or ischaemic penumbra
- Raised ICP due to haematoma expansion, malignant oedema or hydrocephalus
- Infections, commonly chest (due to aspiration from poor swallow) and UTI (due to incomplete bladder emptying from constipation or bed-bound posture)
- Mobility issues such as VTE, constipation, pressure sores
- Mood and cognitive dysfunction which can affect compliance with rehabilitation efforts
- Pain and fatigue due to spasticity, poor sleep posture, inherent result of brain cell damage
- Spasticity/contractures/epilepsy which can impact quality of life
- Swallowing issues, affecting quality of life, and necessitating NGT/PEG tube insertion which can further exacerbate it and cause malnutrition
Stroke: post-event actions?
SECONDARY PREVENTION:
- Clopidogrel 75mg OD (alternatively aspirin plus dipyridamole)
- Atorvastatin 80mg OD (usually delayed > 48 hours)
- Blood pressure and diabetes control
- DOACs or anticoagulants for AF patients; consider left atrial appendage closure if anticoagulants contraindicated
- Addressing modifiable risk factors (e.g., smoking, obesity and exercise)
REHABILITATION:
- Speech and language therapy (SALT) to regain language skills
- Swallowing assessment: consider NGT/PEG tubes if swallowing unsafe (but avoid this in end-of-life patients as risks and discomfort outweigh benefits)
- Dieticians for those at risk of malnutrition
- Physiotherapy (eg: mobility exercises) to regain mobility and minimise spasticity
- Occupational therapy
- Social services
- Optometry and ophthalmology
- Psychology
- Palliation
DISABILITY POST-STROKE:
- Barthel Index (BI) measures disability/dependance in ADL following a stroke
- BI describes 10 tasks, and is scored according to amount of time or assistance required by the patient for each given task
- Total score is from 0 to 100, with 0 being completely dependent, and 100 being completely independent
- BI should be used to assess the functional status of a patient post stroke, and to monitor their improvement with ongoing rehabilitation to regain independence
TIA: principles of management
- Immediate management
- Referral
- AF and CAD cases
- Secondary management and lifestyle
IMMEDIATE MANAGEMENT:
- If suspicion of TIA….
- Aspirin 300mg OD for 14 days; then…
- Clopidogrel 75mg OD as long-term vascular prevention
REFERRAL:
- Referral for specialist assessment < 24 hours (within 7 days if > 7 days since the episode)
- Referral for diffusion-weighted MRI scan as gold standard imaging modality
FOR ATRIAL FIBRILLATION (AF):
- Offer DOACs such as apixaban/rivaroxaban, or other anticoagulants such as heparin/warfarin
- Left atrial appendage closure if above contraindicated
FOR CAROTID ARTERY DISEASE:
- Urgent referral for consideration of carotid endarterectomy if > 50% lumen reduction on carotid USS (according to North American Symptomatic Carotid Endarterectomy Trial (NASCET) criteria)
- Surgery ASAP after diagnosis confirmed
SECONDARY PREVENTION:
- BP control if hypertensive
- Atorvastatin 80mg OD as lipid modification therapy
- Diabetic control if diabetic
- COCP cessation if applicable
LIFESTYLE:
- Smoking cessation
- Exercise initiation
- Diet to avoid salty/fatty/oily foods
- Driving = stop driving if suspected, or confirmed, TIA (1 month for cars and motorcycles, no need to inform DVLA; indefinitely for HGVs, must inform DVLA)
Causes of Ischaemic Stroke?
Embolism: an embolus originating somewhere else in the body (e.g. the heart) causes obstruction of a cerebral vessel, resulting in hypoperfusion to the area of the brain the vessel supplies
Thrombosis: a blood clot forms locally within a cerebral vessel (e.g. due to atherosclerotic plaque rupture)
Systemic hypoperfusion: blood supply to the entire brain is reduced secondary to systemic hypotension (e.g. cardiac arrest)
Cerebral venous sinus thrombosis: blood clots form in the veins that drain the brain, resulting in venous congestion and tissue hypoxia
Causes of Haemorrhagic Stroke?
Intracerebral haemorrhage:
- Bleeding within the brain secondary to a ruptured blood vessel
- Intracerebral haemorrhages can be intraparenchymal (within the brain tissue) and/or intraventricular (within the ventricles)
Subarachnoid haemorrhage:
- Bleeding occurring outside the brain tissue, between the pia mater and arachnoid mater
What are the formally-recognised subtypes of stroke?
BAMFORD/OXFORD CLASSIFICATION:
- Total Anterior Circulation Stroke (TACS)
- Partial Anterior Circulation Stroke (PACS)
- Posterior Circulation Syndrome (POCS)
- Lacunar stroke (LACS)
OTHER RECOGNISED PATTERNS:
- Wallenburg’s syndrome/Lateral medullary syndrome = ipsilateral ataxia, nystagmus, dysphagia, facial numbness and Horner’s syndrome; contralateral limb sensory loss (infarct is in ipsilateral posterior inferior cerebellar artery)
- Weber’s syndrome = ipsilateral CN III palsy and contralateral weakness (infarct is in branches of the posterior cerebral artery)
Total Anterior Circulation Stroke (TACS):
- Definition
- Clinical criteria/presentation
DEFINITION:
- A large cortical stroke affecting the areas of the brain supplied by both the MCA and ACA
CLINICAL CRITERIA/PRESENTATION:
(all 3 of the following)
- Unilateral weakness and/or sensory deficit of the face, arm and leg
- Homonymous hemianopia
- Higher cerebral dysfunction (dysphasia, visuospatial disorder, neglect, agnosia)
[All 3 need to be present to diagnose TACS]
Partial Anterior Circulation Stroke (PACS):
- Definition
- Clinical criteria/presentation
DEFINITION:
- A less severe form of TACS
- Only part of the anterior circulation is compromised
CLINICAL CRITERIA/PRESENTATION:
(any 2 of the following)
- Unilateral weakness and/or sensory deficit of the face, arm and leg
- Homonymous hemianopia
- Higher cerebral dysfunction (dysphasia, visuospatial disorder)*
*Higher cerebral dysfunction alone is also classified as PACS.
Posterior Circulation Syndrome (POCS):
- Definition
- Clinical criteria/presentation
DEFINITION:
- Damage to areas of the brain supplied by the posterior circulation (ie: cerebellum and brainstem)
- Vertebrobasillar artery involvement
CLINICAL CRITERIA/PRESENTATION:
- Cranial nerve palsy AND a contralateral motor/sensory deficit
- Bilateral motor/sensory deficit
- Conjugate eye movement disorder (inability to move both eyes together in a single horizontal or vertical direction, such as horizontal gaze palsy)
- Cerebellar dysfunction (e.g. vertigo, nystagmus, ataxia)
- Isolated homonymous hemianopia
[Any one of the following need to be present for a diagnosis of a POCS]
Lacunar Stroke (LACS):
- Definition
- Clinical criteria/presentation
DEFINITION:
- A subcortical stroke occurring secondary to small vessel disease
- Often linked with cardiovascular disease (eg: hypertension, diabetes, hypercholesterolaemia etc)
- No loss of higher cerebral functions (eg: dysphasia)
CLINICAL CRITERIA/PRESENTATION:
- Pure sensory stroke
- Pure motor stroke
- Sensori-motor stroke
- Ataxic hemiparesis
[Any one of the following needs to be present for a diagnosis of a LACS]
Stroke Mimics: examples and classification?
EASILY RECOGNISABLE ON IMAGING:
- Space-occupying lesions
- Multiple sclerosis (optic neuritis is often first sign, limb numbness/tingling, weakness, cerebellar symptoms)
- Subdural hematoma (headache, trauma etc)
DISTINCT NON-STROKE CLINICAL FEATURES, AFTER CLINICAL EXCLUSION:
- BPPV (dizziness, vomiting, episodic and transient vertigo, imbalance)
- Vestibular neuronitis (dizziness, recent URTI, nausea and vomiting)
- Transient global amnesia (abrupt onset, asks pertinent questions repeatedly, unable to recall the episode, no focal neurological symptoms, disoriented to time and place)
- Syncope
REQUIRES ADDITIONAL INVESTIGATIONS:
- Migraine with aura
- Hemiplegic migraine
- Seizures (focal or not)
“APPARENT” NEUROLOGICAL DEFICITS:
- Postural hypotension
- Hypoglycaemia
- Infection and sepsis
- Hypoxia
- Fatigue
National Institute of Health Stroke Scale (NIHSS):
- Definition
- Interpretation of values
DEFINITION:
- A systematic assessment tool providing a quantitative measure of stroke-related neurological deficits
- Used to assess the severity of a stroke, selection for various acute therapies and estimate prognosis and recovery
INTERPRETATION OF VALUES:
0 = no stroke
1–4 = minor stroke
5–15 = moderate stroke
16–20 = moderate/severe stroke
21–42 = severe stroke
Stroke: pathophysiology at the cellular level and clinical relevance
PATHOPHYSIOLOGY AT CELLULAR LEVEL:
- Hypoperfusion in the endothelial lumen causes depletion of available ATP, leading to impairment of energy-dependent cellular processes, especially that of membrane transport
- Membrane transport is responsible to the generation of action potentials (AP), which in turn drive all neuronal transmission
- APs are binary (ie: on or off)
- Therefore, when ATP levels in an available vascular territory drop below the threshold necessary to sustain AP activity, AP cessation occurs and neuronal transmission ceases
CLINICAL RELEVANCE:
- Neurological disturbance of sudden onset (reflecting AP cessation)
- Focal syndromes of stroke (as only neurovascular units in the relevant vascular territory are affected)
- Predominantly negative syndromes of stroke (reflecting the loss of function due to AP cessation)
Stroke: principles of thrombolysis?
THROMBOLYSIS:
- IV alteplase (tissue plasminogen activator, tPA) or
- Mechanical thrombectomy
IV ALTEPLASE:
- For disabling stroke presenting < 4.5 hours
- Fibrinolytic drug which activates plasminogen to form plasmin, that degrades fibrin and so breaks up thrombi
- Initiate aspirin 300mg OD for 14 days thereafter
[NB: expect D-dimer to increase following tPA use]
COMPLICATIONS OF THROMBOLYSIS:
- Adverse effects of alteplase (eg: bleeding, oedema, anaplylaxis)
- Evolution of stroke causing raised ICP (eg: oedema, hydrocephalus)
- Seizures
- Infection
- Metabolic disturbances
Stroke: principles of mechanical thrombectomy?
MECHANICAL THROMBECTOMY:
- For large vessel occlusion (eg: ICA, MCA, BA, VA)
- For NIHSS score 6 or more
- Presentation < 6 hours
- For pre-stroke MRS 0 or 1
Stroke: principles of decompressive hemicraniectomy (DHC)?
INDICATIONS:
- Malignant oedema in younger patients (<60 years old)
- Can also be considered in biologically fit stroke patients above this cut-off
- Preserves life in the context of significant dependancy by virtue of being required in patients with major strokes
CRITERIA FOR DHC:
- Referral to neurosurgery should be done within 24 hours of onset
- Surgery should be done within 48 hours of onset
Stroke: principles of antithrombotic therapy? (ie: anticoagulations and antiplatelet agents)
INDICATIONS:
- Immediate administration of antiplatelet agents is standard practice in all suspected TIAs, confirmation of ischaemic stroke and 24 hours after thrombolysis
- Applies in those with AF, severe LV dysfunction, thrombophilia and venous sinus thrombosis
EXAMPLES OF DRUGS:
- Aspirin
- Clopidogrel
- DOACs
- Warfarin
- Heparin (IV or SC)
RELEVANT INVESTIGATIONS:
- ECG to diagnose AF, LV dysfunction etc
- Holter to diagnose paroxysmal AF
- ECHO to diagnose anatomical heart pathology
- Thrombophilia screening
Stroke: principles of carotid endarterectomy (CEA)?
PRINCIPLES OF CEA SURGERY:
- Symptomatic carotid disease (eg: after a TIA or stroke with good recovery)
- Atherosclerosis in the carotid artery may be the source of emboli in some patients
- 50% lumen reduction on carotid ultrasound (North American Symptomatic Carotid Endarterectomy Trial (NASCET) criteria)
- Surgery ASAP following symptoms
OTHER RELEVANT MEDICAL INTERVENTIONS:
- BP control for hypertension (aim < 130/80mmHg)
- Statin therapy at high doses
- Dual antiplatelet therapy
[NB: medical intervention is to achieve plague stabilisation]
Stroke: principles of nasogastric and percutaneous endoscopic gastrostomy (PEG) feeding?
PRINCIPLES:
- Nutritional support for recovering stroke patients due to unsafe swallow function, pending return of safe swallow
HOW TO ASSESS SWALLOW FUNCTION:
- Video fluoroscopy
- Flexible endoscopic evaluation of swallowing (FEES)
CONTRAINDICATIONS OF NGT/PEG:
- End of life patients, due to them being subjected to the risks of tube feeding without any meaningful gains in the goals of minimising symptoms and improving QoL to prevent death
Prognostic factors for stroke patients? (good and bad)
GOOD FACTORS:
- Absence of coma
- Early motor recovery
- Continence
POOR FACTORS:
- Severe communication deficit
- Old age
- Incontinence
- Neglect
- No leg movement after 2 weeks
- Severe upper limb weakness at 4 weeks
Some issues faced during stroke rehab?
APHASIA/DYSARTHRIA:
- About 1/3 of people will be affected
- Refer SALT
UNSAFE SWALLOWING:
- Refer for swallowing assessment with dietician input
- NGT/PEG feeding within 24 hours
- Gastrostomy feeding it they cannot tolerate NGT feeding or unable to take solids and liquids 4 weeks post-stroke
MALNUTRITION:
- About 25% of patients will be affected
- Consider NGT and PEG feeding with dietician input
- Review oral mouth care
BALANCE AND WALKING:
- Weakness will affect 80% of patients
- Physiotherapy should be involved to train patients in the use of mobility aids, with lower-limb strengthening exercises and task specific training
INCONTINENCE:
- Timed toileting
- Review caffeine intake
- Bladder training
- PFMT training
- Medication review (eg: minimise constipating drugs)
SPASTICITY AND CONTRACTURES:
- Affects up to 25% of patients
- Physiotherapy input for simple exercises such as positioning, passive movement and/or pain control
- IM botulinum for focal spasticity
- Baclofen/tizanidine (skeletal muscle relaxants) for generalised spasticity
COGNITIVE IMPAIRMENT:
- Associated with poorer outcomes such as longer hospital stays and dependance
- Involve clinical neuropsychologist
ANXIETY AND DEPRESSION:
- Refer psychiatry
- Consider social interaction, increased exercise and group therapy etc
FATIGUE:
- Common
- Assess for mental/physical factors
Transient Global Amnesia:
- Definition
- Risk factors
- Presentation
- Investigations
- Management
DEFINITION:
- A temporary, anterograde amnesia with an acute onset that usually occurs in middle-aged and older individuals
- Diagnosis of exclusion
- Stroke mimic, often cause of presentation to TIA clinic following GP referral
RISK FACTORS:
- Middle age
- Ischemic heart disease
- Hyperlipidemia
- Migraines (or headaches)
PRESENTATION:
- Acute onset of several hours of memory loss
- Repetitive questioning
- No recall of how they got where they are or what they did in the time immediately preceding the onset
- No LOC
- SHX of preceding vigorous exertion, coitus, or severe stress (emotional or physical)
- Complete resolution within 24 hours
O/E:
- Often cannot recall events leading to admission, or events of the circumstances
- Neurological examination unremarkable, no focal neurological deficits
INVESTIGATIONS:
a) Bedside
- BM to exclude hypoglycaemia
- ECG to exclude AF as a risk factor for stroke/TIA
b) Bloods
- U&Es to exclude electrolyte imbalances
- LFTs to exclude alcoholism and wernicke’s encephalopathy
- HbA1c for diabetes as stroke risk factor
- Lipid profile for hypercholestrolaemia as stroke risk factor
c) Imaging
- CT head exclude acute stroke
- MRI head to exclude TIA if appropriate
MANAGEMENT:
- Admit until amnesia resolves
- Supportive treatment
- Consider thiamine against Wernicke’s encephalopathy
Hypoglycaemia
